Branca Jacopo J V, Fiorillo Claudia, Carrino Donatello, Paternostro Ferdinando, Taddei Niccolò, Gulisano Massimo, Pacini Alessandra, Becatti Matteo
Department Experimental and Clinical Medicine, Anatomy and Histology Section, University of Firenze, 50134 Firenze, Italy.
Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Firenze, 50134 Firenze, Italy.
Antioxidants (Basel). 2020 Jun 5;9(6):492. doi: 10.3390/antiox9060492.
Cadmium (Cd), a category I human carcinogen, is a well-known widespread environmental pollutant. Chronic Cd exposure affects different organs and tissues, such as the central nervous system (CNS), and its deleterious effects can be linked to indirect reactive oxygen species (ROS) generation. Since Cd is predominantly present in +2 oxidation state, it can interplay with a plethora of channels and transporters in the cell membrane surface in order to enter the cells. Mitochondrial dysfunction, ROS production, glutathione depletion and lipid peroxidation are reviewed in order to better characterize the Cd-elicited molecular pathways. Furthermore, Cd effects on different CNS cell types have been highlighted to better elucidate its role in neurodegenerative disorders. Indeed, Cd can increase blood-brain barrier (BBB) permeability and promotes Cd entry that, in turn, stimulates pericytes in maintaining the BBB open. Once inside the CNS, Cd acts on glial cells (astrocytes, microglia, oligodendrocytes) triggering a pro-inflammatory cascade that accounts for the Cd deleterious effects and neurons inducing the destruction of synaptic branches.
镉（Cd）是一种I类人类致癌物，是一种广为人知的环境污染物。长期接触镉会影响不同的器官和组织，如中枢神经系统（CNS），其有害影响可能与间接产生活性氧（ROS）有关。由于镉主要以+2氧化态存在，它可以与细胞膜表面的大量通道和转运体相互作用以进入细胞。本文综述了线粒体功能障碍、ROS产生、谷胱甘肽耗竭和脂质过氧化，以便更好地表征镉引发的分子途径。此外，还强调了镉对不同中枢神经系统细胞类型的影响，以更好地阐明其在神经退行性疾病中的作用。事实上，镉可以增加血脑屏障（BBB）的通透性并促进镉的进入，进而刺激周细胞维持血脑屏障开放。一旦进入中枢神经系统，镉就会作用于神经胶质细胞（星形胶质细胞、小胶质细胞、少突胶质细胞），引发促炎级联反应，这是镉产生有害影响的原因，并且会导致神经元突触分支的破坏。
